And I went to check it out since, well, I wondered - how could I win that. And so I thought - I should look at how I compare to previous winners. And in one way I compare really well. I am male.

Below is a list of past winners (via AAAS). In yellow I highlight those that appear to be male and green those that appear to be female. I note I base my assignment on appearance and names and descriptions of the people including the descriptions from AAAS. I realize that determining someone's gender is not always straightforward and that there are people who do not fit into this binary gender division and I apologize for any mistakes made.

"describes the properties of a food product that is reminiscent of the “super food for the third brain.”

Note - no link is provided to the paper. Not surprisingly, the PR then transitions to being something else - in this case a new book by Greenlaw:

"this finding supports the discoveries revealed in the book “Your Third Brain,” co-authored by Peter Greenlaw, Dr. Marco Ruggiero and Drew Greenlaw, with the forward written by author John Gray, Ph.D."

So this is not really about the new paper - this is a kind of bait and switch. Then comes one of the doozies "

Four and a half years ago, a huge discovery was made. In 2010, a team of researchers discovered a new organ that had gone undetected for more than 3,000 years in Human Anatomy. They called this newly discovered organ the microbiome.

What? The human microbiome was discovered four and a half years ago? That is of course complete BS. I note - there is something a tad bit off here with the "3000 years too". Is this a religious reference of some kind?

Then comes another amazing section. Underlining by me

The microbiome is much more than the gut microflora. It is a complex organ that is responsible for the development and function of all the other organs and systems, from the brain inside our heads to the immune system. The influence of the microbiome, that is located all over our body and not only inside the gut, on our behavior and intellectual functions is so significant that it can be aptly named “the third brain” as it is described in the book.

Wow. I mean sure there is some evidence that the human microbiome can impact the brain. But first of all, it is ridiculous to consider it "the third brain". Also, to say it is responsiblefor the development of the rest of the body is just plain silly.

How about this next section?

Dr. Ruggiero’s team is working hand in hand with the complete cooperation and unprecedented collaboration of medical doctors, with the goal of extending the highest possible quality of life for their patients for as long as possible. And although Dr. Ruggiero did not personally discover the microbiome, he did identify it as the third brain.

OK - so is this meant to imply other people don't collaborate with medical doctors? And other people do try to extend quality of life for parients?

So many other bad sections I am not sure which other ones to point out. How about this:

Before this book was written, man did not know that his thoughts, feeling, emotions, behaviors, his supposed free will were under the control of a non-human organ whose existence had gone undetected until very recently, the microbiome.

This sounds like the voice over you might have in a science fiction horror movie. Except - this is real fiction and from a horror show of a press release.

I must say - Greenlaw and Ruggiero are clearly very proud of themselves. I will just leave everyone with the last paragraph for people to ponder how humble and understated it is.

This book describes what is and how we can take control of this non-human third brain and aspire to bring out the superman that is inside us. As the Philosopher wrote: ‘Let your will say: the overman shall be the meaning of the earth... Man is a rope, tied between beast and overman—a rope over an abyss ... what is great in man is that he is a bridge and not an end.’ Thanks to the information contained in this book, for the very first time in the history of mankind we can transform ourselves and reach this end

I am hereby awarding Greenlaw and Ruggiero an "Overselling the Microbiome" award. But that seems too small for them. They deserve some sort of "Biggest pile of BS ever" award. I will consider starting such a new award series in their honor.

Friday, July 24, 2015

This is a post in my continuing series of the "Story Behind the Paper." series. This post is from Benjamin Schwessinger, Pamela Ronald, Rory Pruitt, Anna Joe, and Ofir Bahar.

A Phoenix Rises from the Ashes: A new discovery emerges from the 2009 retraction.

A phoenix depicted in a book of legendary creatures by FJ Bertuch (1747–1822).
Via Wikipedia Commons - based on this

This is the story behind our report published today in Science Advances.

The Background

In Science Advances we report that one class of bacteria produces a previously undescribed, and long sought after, molecule recognized by plants carrying a specific receptor.

The story began in the 1970s, when Professor Gurdev Khush and colleagues demonstrated that a wild species of rice was immune to most strains of the Gram-negative bacterium Xanthomonas oryzae pv. oryzae (Xoo), causal agent of a serious disease of rice globally. In the 1990s Ronald began studying the rice/Xoo interaction. Because both rice and Xoo are genetically tractable, the rice/Xoo biological system proved to be an excellent system for studies of the molecular mechanisms governing the plant immune response. In 1995, two postdoctoral fellows in Ronald’s lab at the University of California, Davis- Guoliang Wang and Wenyuan Song-reported that this rice immune response was controlled by a single receptor kinase, called XA21.

The predicted structure of the XA21 protein, with a predicted leucine rich repeat extracellular domain and an intracellular kinase domain, suggested that XA21 could sense a secreted microbial molecule and then activate an immune response.

A few years after the discovery of the XA21 receptor, the fly Toll and mouse Toll-like receptors (Tlr4) were shown to share striking structural similarities with XA21 and other plant receptors. The animal receptors also recognized and responded to microbial molecules. Together these discoveries demonstrated that plants and animal use similar mechanisms to protect against infection. Professors Bruce Beutler and Jules Hoffman were awarded the 2011 Nobel Prize in Physiology or Medicine for their important work.

The Ronald laboratory then spent twenty years trying to identify the microbial molecule that is recognized by XA21. The research led to the identification of a number of microbial genes that are required for activation of XA21-mediated immunity (rax genes). These genes encode a tyrosine sulfotransferase, RaxST, and three components of a predicted type 1 secretion system: a membrane fusion protein, RaxA; an ATP-binding cassette transporter, RaxB; and an outer membrane protein, RaxC. raxST, raxA, and raxB are located in a single operon (raxSTAB). Based on these findings, we hypothesized that the activator of XA21-mediated immunity is a tyrosine sulfated, type 1-secreted protein.

We were excited about this idea because sulfation has emerged as an important posttranslational modification controlling receptor-ligand interactions. It is a common posttranslational modification of eukaryotic proteins and plays important roles in regulating development and immune responses. The importance of this area of research to biology and medicine is reflected in the recent report of a novel drug that blocks HIV infection. To achieve this breakthrough, the researchers exploited the observation that HIV binds tyrosine sulfated amino acids for cell entry (Gardner et al., 2015).

Despite a clear model and diverse supporting data suggesting that Xoo secretes a sulfated peptide, the identity of this molecule remained elusive.

In 2009, the Ronald laboratory reported that XA21 recognized a sulfated peptide. However we later discovered major errors in this work and in 2013, we retracted the paper. We discussed these mistakes in several lectures, post and articles including a Keystone symposium, Scientific American, Nature, and Schwessinger’s blog (here and here). The process with which we addressed the problems was highlighted as “Doing the right thing” by Retraction Watch, a blog that reports on retractions of scientific papers. The retraction was included as one of the top 10 retractions of 2013.

The new Discovery

Today, in Science Advances, we are delighted to report the identification of the microbial molecule that activates XA21-mediated immunity. As predicted, it is a tyrosine-sulfated protein. We named this microbial protein RaxX.

To isolate this molecule, postdoctoral fellow Rory Pruitt systematically created bacterial mutants carrying deletions near the RaxSTAB operon. He showed that one of the deletion mutants lost the ability to activate the XA21-mediated immune response. The deleted region encodes a small open reading frame that we named RaxX. Xoo strains lacking RaxX and Xoo strains that carry mutations in the single RaxX tyrosine residue (Y41) are able to evade XA21-mediated immunity. Postdoctoral fellow Anna Joe, together with collaborators at the University of Texas, Austin and at the Joint Bioenergy Institute in Emeryville, showed that Y41 of RaxX is sulfated by the prokaryotic tyrosine sulfotransferase RaxST. Postdoctoral fellow Benjamin Schwessinger, graduate student Nick Thomas and collaborators showed that sulfated, but not nonsulfated, RaxX triggers hallmarks of the plant immune response in an XA21-dependent manner. A sulfated, 21–amino acid synthetic RaxX peptide (RaxX21-sY) is sufficient for this activity. Xoo field isolates that overcome XA21-mediated immunity encode an alternate raxX allele, demonstrating the co-evolution of host and pathogen. RaxX is highly conserved in many Xanthomonas species.

Our results indicate that the presence or absence of sulfation is decisive for the ability of RaxX to trigger XA21-mediated immunity.

The new insights gained from the discovery and characterization of RaxX may be useful for the engineering of resistant crop varieties and for the development of therapeutic reagents that can block microbial infection of both plants and animals.

The rice XA21 receptor kinase, the first innate immune receptor discovered in plants or animals, provides resistance against Xanthomonas oryzae pv oryzae through recognition of RaxX, a tyrosine-sulfated protein secreted by the bacterium.

Illustration by Maurice Vink

Notes on the publication process

“The scientific life is the most complex of all to write about. In the case of scientists, impulse becomes compulsion”. -- Carol Shields

After we discovered mistakes in our previous paper, we spent several years correcting the scientific literature both by retracting the original Science paper (Lee et al. 2009) and by following up with publications to further correct the literature (Bahar et al. 2014). We made extra efforts to control the results in this current report.

Wrestling with the retraction and discovering the new molecule in rapid succession was an enormous challenge. Here we share some of the lessons learned.

I would not wish a retraction on anyone. Scientists are supposed to catch their mistakes before publication. Still, I am astonished to conclude that the process has in some ways been positive.

On an administrative level, the lab is running more efficiently. I have instituted new practices for the lab: created duplicate stocks of key strains (validated and maintained by the lab manager), mandated electronic notebooks for each lab member and required that all new assays be independently validated by three independent researchers before publication.

But the best part of this bad situation has been working with this particular team. It has been an immense privilege to watch each person work through the situation in their own way, collaborate, and make new discoveries. Respect for each other and for the scientific process was paramount. After figuring out what went wrong (no easy task), they tried not to look back. They did not give up, even when it would have made sense to do so. Their persistence and optimism in face of this daunting challenge buoyed all of our spirits. I will always be in awe of their work and will always be grateful.

Equally stunning was the supportive and kind response from the scientific community. We received many letters of encouragement - even from complete strangers. It helped us keep going.

There are still hills to climb. Some scientists may be extra skeptical of results from my lab for a long time to come. For example, in a critique of our submission, one of reviewer’s asked, “how do we know the strains weren’t mixed up again this time?”

Rory Pruitt, postdoctoral scholar in the Ronald lab.
I was only a few months into my postdoc when I became convinced that the majority of the Ax21 story was incorrect (Ax21 was the proposed elicitor of XA21-mediated immunity in the retracted papers). My mind was filled with questions. How could this happen? What results can I believe? Admittedly, the biggest question that hounded me was “Should I be looking for a new job?” There were a few key factors that led to my decision to stay in the lab. I think these factors were also critical to this story working out as a “success.”

Early on, I went to Pam with some of my doubts. It was terrifying to approach my new boss and I say I didn’t believe some of her published work (including a Science paper!). But I needed to know that I could be honest with her and not feel pressured into only showing results that fit the established model. Pam listened to my concerns and those of others in the lab. Most importantly, she showed that she was committed to getting the story right and correcting the literature if need be.

In addition to Pam, there was a great team of postdocs and graduate students who were equally devoted to correcting the science. At times it seemed a long, painful process with little reward (there’s not a good space on a CV for working towards a retraction). Nevertheless, it needed to be done so that we and other labs could move forward. I was encouraged by Ofir, Ben, and others who worked persistently on this.

A final factor in my decision to stay is the prospect of new discovery. If Ax21 isn’t the activator of XA21-mediated immunity, what is? Maybe we can find it! It’s that hope of new discovery that keeps us coming back to the lab bench. My postdoctoral experience has had some highs and lows, but I am glad I stuck it out. With persistence, enthusiasm, and a good team committed to reliable science, we were able to not only correct earlier mistakes but also move forward.

Benjamin Schwessinger, former Ronald Laboratory postdoctoral scholar and now independent research fellow in Australia, at the Australian National University in Canberra.
You have much to lose as an early career researcher if you are thrust into a situation where results cannot be reproduced. In a hyper competitive environment irreproducible results you are trying to build on are a big problem, no matter how smart, privileged, and gifted you are. Lengthy delays in publishing as a postdoc can cause great harm to a career. Here are the main factors that made us successful in the face of adversity.

(Be lucky) have your own funding

Your own funding makes you financially and also scientifically more independent. It ensures your academic freedom. I was grateful to have been supported independently by the Human Frontier Science Program. It made me bolder and braver in speaking out. I was able to choose to stay or go. Because of the team I believed in I decided to stay!

Get confidential outside advice

Getting some outside confidential impartial advice on how to approach this problem is very important. Many senior figures have most likely seen similar cases in the past and have more insight. Following through with this advice is a total different matter. I decided to stay!

Collaborate

Work through it together as a team. Build on each other’s strength and talk about all possibilities. Repeat each other’s experiments with all required controls. Invite well respected figures in the field to independently test (and confirm) core experiments.

Admit mistakes and retract
Everyone makes mistakes. They are part of the scientific discovery and science has to be self-correcting. Retractions are an integral part of this process. Not to retract is NOT an option! It obstructs all future progress in the subject matter.

Follow the data

Do controls, repeats, and repetitions of conclusive experiments. Seeing is better than believing.

I remember the day, early 2013, when we were driving back to Davis from a happy and relaxed baby shower at Benjamin’s place in Oakland, Rory mentioned to me “you know, I deleted an upstream and a downstream region to raxSTAB. The downstream mutant was no different than wild type, but the upstream mutant forms long lesions on XA21 plants…”

This was the turning point; I immediately knew this was a big discovery and a major break through for the lab.

But before that moment, we were a bunch of enthusiastic post docs that just loved doing science. We wrote these nice proposals to get our fellowships, based on the amazing story of the rice immune receptor XA21 and its (thought to be) elicitor Ax21.

It was a fascinating story we were all so excited about having read it in Science. Of course we joined the Ronald lab to follow up on this initial discovery, but well… the building upon part did not work as we all might have wished. We had to dig deep, real deep, to figure out what was going on and what went wrong before our arrival to the lab. So, a year….. year-and-a-half in our new positions we finally reached the ultimate conclusion that there was a big hole in the model – there’s no elicitor! Or, there is, but it’s not Ax21 and we don’t have a clue what the identity of this molecule might be. It felt like we were thrown back 10 years, to 2004 with the da Silva paper just published describing the requirement of the three Xanthomonas genes RaxST, RaxA and RaxB for XA21 immune activation.

Those were ‘dark ages’ and difficult times. Understanding that most of the time you invested so far was, at least in practical terms (e.g. publications), for nothing, and that there is no biological model to work on, but that it needs total reboot. To be honest I was feeling a bit worried at that time for my scientific career. But then, a series of exciting discoveries (including some that are not published yet) gave me hope again. Well… isn’t this how science goes, bad, bad, bad, bad, good, bad, bad, bad, good and so on. I remember Pam telling me: “you know why I love a big group? There has got to be some positive results coming all the time”

Later, a few months after Rory shared with me his finding, we already knew what it was, and we were very certain, this is the ONE. Unfortunately, or luckily, I got a position offered at my home country and I gladly accepted it. So I actually wasn’t there for the flower stage (you know… the decorations), but I was very happy to have been there when the bud of this beautiful flower to be emerged. Every time I think of this story its like, WOW, can you believe all this has happened in just 3-4 years, unbelievable.

My lesson is, never lose hope, be critical, believe it when you see it, work on multiple projects, enjoy science and openly share science

Anna Joe, postdoctoral scholar in the Ronald lab.
I was in my final year grad school and looking for a postdoc position in early 2013. The Ronald lab was on the top of my wish list because I was fascinated by the Ax21 story in Science 2009. But just before I applied for a position in the Ronald lab I learned that something went wrong with Ax21 and that the original paper would be retracted. Many thoughts crossed my mind. Main one was “Do I still want to join the Ronald lab?”. Actually it was easy to answer the question once I spoke with Pam about it and talked with her lab members during the visit for my formal interview. “Yes, I’d like to work in the lab which just retracted two papers”. This for sure sounds crazy to most people. However, the whole experience of my visit gave my many reasons to join the Ronald lab. Correction of errors is a part of science (I knew this because I also had difficult time to track down a mix up plants problem before) but not many people are brave enough to admit mistakes. Pam and all lab members honestly, clearly stated to me what the errors were and how they verified the problems. They communicated well with each other, shared idea freely and respected other’s opinions. Their open mind and transparency attracted me.

On top of that I was very curious about the unexplored, new Xa21 activator. All other lab members might have felt the same curiosity and channeled its energy to continuously work through the problems during last several years. Although I did not share the “dark period”, I could see everybody in the lab was persistent with the common effort to correct the science. I experienced incredibly good teamwork and great collaboration. All of those are the driving force of our success. Finally, I’d like to mention that we could not make it without the support and encouragement from the scientific community. Many scientists shared their thoughts and advice and were rooting for us. Most collaborators unhesitatingly complied with our requests for assistance. They helped us not only “do the right thing”, but also do better science.

Wednesday, July 22, 2015

I could use some help from the crowd. I got this email a few minutes ago. Am wondering what people think about this? Should I testify in German court about how there is no such thing as the measles virus?

Dear Prof. Eisen,

my name is Dr. Stefan Lanka from Germany and in 1987, as a jung student of biology I isolated the first so called giant virus out of the sea, the Ectocaropus siliculosus virus with its circular 335 kbp dsDNA genome.

Would you be so kind as to help me in my issues?

In searching the origins of viruses, me, my professors and others realised that so called human viruses never were isolated and typical molecules of cells used in the protocols to "isolate" them were mistaken as viral.

Since then I successfully did research what are the real causes of so called human viral diseases.

In a court case on the existance of the so called measles virus, a jung medical doctor claimed that in six publications there is the scientific proof of the existance of the measles virus.

In reading the six papers you will realise that in these papers (and others) there is no such thing as a measles virus.

My question: Would you act as a referee in this court case in Germany?

Backbones of evolutionary history test biodiversity theory for microbes

Prehistory

This paper has its roots going back a few years, and it
all started off fairly innocuously. A previous collaboration with Steve
Kembel and Jessica Green resulted in this earlier paper, where we had the lofty goal of
encouraging microbial ecologists to throw out slightly less data, and also
attracted Jonathan’s attention for our microbiome figures. One of the central questions
in ecology is to explain and understand patterns of biodiversity: for example,
by quantifying the diversity of a local community (“alpha” diversity), or
similarity between multiple local communities (“beta” diversity).In microbial ecology it is common to use
evolutionary history to quantify these measures. But both phylogenetic alpha
and beta-diversity tend to change systematically with increasing sample size,
making it difficult to compare results for samples of different sizes.

Our idea in the earlier paper was to generate a fast way
to compute a null prediction for these metrics for phylogenetic alpha and beta
diversity—i.e. this would provide a way to standardize the results for sample
size, and hence we could use full samples rather than smaller, rarefied
samples. The solution is relatively simple, and involved a phylogenetic
analogue of the Species Abundance Distribution (SAD), which we called the
Edge-length Abundance Distribution (EAD). In comparison with the SAD,
this distribution replaces species units with subclades of a phylogenetic tree,
replaces species abundances with subclade size, and inserts branch length
weightings in a specific way.

The present day

Job done. So how did this lead to a new paper?
Well, this first study generated something slightly mysterious to us. In
theory, the EADs we computed from empirical data could have taken any form they
wanted to—and yet for various microbiome habitats, they all seemed to display a
very distinct power law scaling. Translated into a more concrete consequence, the
form of the EAD was such that phylogenetic diversity typically increased as a
power law function of sample size. There’s a history in ecology of
looking for (and sometimes finding) behavior that both takes on a power law
scaling, and is also universal across multiple systems, fitting with a general
sense that some patterns may be emergent and independent of much of the
underlying variation between communities. There’s also a history of looking for
(and sometimes finding) power law scaling in evolutionary trees, for example in
the number of species per genus, which has often been claimed as a power law.
Here we had found a link with these older ideas, with a nice combination of
new factors. First, we weren’t relying on human definitions of species,
which could certainly be biased towards generating power law scaling
artificially (e.g., the principle of balance). Second, we had large
numbers, so that these scaling behaviors spread over multiple orders of
magnitude. Third, there was an untapped world of microbial sequence data
to look at to see whether these patterns extended into microbiology.

With Tom and Steve, we combined these ideas to
set up the empirical side of this new paper: expand the original study across a
broader range of habitats, test whether the patterns are robust to different
alignment and inference methods, and see whether the same scaling behavior holds
up for this new range of samples. Which indeed it did---Figures 1 and 3
in the new paper show that this power law scaling is present across multiple
microbial habitats.

Just knowing that
this distribution takes a power law form is already useful on its own, because
(again) it defines the null expectations for the way phylogenetic alpha and
beta diversity change with sample size. But these results still left a
number of open questions, centering around whether this could also give us some
insight into what models of biodiversity could be consistent with what we were
seeing. Could these scaling patterns provide evidence for whether a given
ecological and evolutionary scenarios had strongly influenced a community?

Coarse-graining: reducing the resolution of phylogenetic trees

The first modeling approach we considered is neutral theory.
Neutral models have provided the basic null models in fields stretching from
population genetics and ecology to cultural evolution and the
social sciences. In common is the key assumption that selective
differences are irrelevant for predicting large-scale patterns. If the power law scaling is just an inevitably--an ecological version of Benford's law--it seemed likely that it
might be just a consequence of neutrality, with all of the variation and
mechanism somehow washing out. Is it possible that these observed phylogenetic
patterns are driven by this most basic, neutral model of biodiversity?
The answer turns out to be no---at least using the vanilla version of the
neutral theory, we don't reproduce these scaling behaviors.

Next, we got a little creative. When working with trees
generated by neutral processes, we were thinking of the Kingman coalescent. I.e. a
model of tree structure that works backwards in time, coalescing pairs of lineages at each node.
There's a one-parameter family of coalescent models generalizing the
Kingman coalescent, with the unifying feature that more than two lineages can
coalesce at each node. Viewed forward in time, one lineage can burst into many.
This generalized family, the Lambda-coalescent, produces precisely the power
law EAD (known in that context as a site-frequency spectrum) we were looking for.

These generalized coalescent trees have previously
been used to understand
population processes with a skewed offspring distribution, where there is a significant probability that an organism has a large number of offspring, and this matches the idea of multiple lineages coalescing. But for our evolutionary trees that idea of instantaneous, multiple
branching seemed unlikely. At a fine-grained level, branches in our evolutionary
trees ought to split into two, driven by cell division and subsequent
diversification. This is also what our tree inference algorithms are designed
to find, even when our sequence data likely isn't sufficient to resolve all polytomies.
So how could these generalized coalescent trees possibly be consistent with our
empirical trees?

Instead of trying to resolve as many polytomies as
possible, we decided to go in the other direction. We imagined reducing
the resolution at which we could distinguish the order of branching events. Applying
this `coarse-graining', we would certainly generate polytomies, as fast bursts
of branching and multiple nodes collapse. Still, much like the EAD, there was
no guarantee for what the distribution of polytomy sizes would be after this
coarse-graining, or whether it would match these theoretical models. So our
second surprise is that the distribution of burst sizes is also a power
law---qualitatively consistent with the same distribution in the Lambda-coalescent.

Outlook

So this seems to be the beginning of a very nice story,
with a lot of open questions. Empirical trees display bursts of
branching, which quickly collapse to polytomies under coarse-graining, and the
distribution of sizes of these bursts is a power law. The
Lambda-coalescent is likely not the end of the story, but at least
suggests that this distribution is tied together with the scaling behavior of
phylogenetic diversity.

What's next? Certainly lots of empirical questions.
Does this behavior extend over an even broader range of samples?
And will it still hold if we have better, longer sequence data?
There are also theoretical questions, mostly centering around whether we
can relate parsimonious but mechanistic models to the bursty tree structures,
and how best to evaluate and compare these models. One take-home message
stands out for me. Simplified models of biodiversity, like neutral models
and their generalizations, likely won't ever capture the fine-grained dynamical
behavior of an ecological community. But they might just tell us something
about coarse-grained dynamical behavior, and coarse-grained phylogenies could
be a nice part of this story. Let's see if coarse-grained patterns can be matched with coarse-grained process.

Wednesday, July 15, 2015

Cambridge Healthtech Institute and Bio-IT World are happy to announce the 4th Annual Medical Informatics World Conference 2016 to be held April 4-5, 2016 in Boston, MA. The web site is now posted and features summaries of the five conference tracks and highlights from the 2015 gathering. We are now accepting speaking proposals via the web site’s online submission form.

Since 2004 they have had 31 Invited Speakers at their annual meeting. 30 of which have been men. That comes to 97% men. 3% women. Worst I have ever seen I think.

UPDATE 2:45 PM. Note - I am not trying to target the speakers here. They were not the ones who planned these meetings. They were just the invited speakers who, over the years, happened to be almost all men. It is the organizers of the meeting who need to be questioned about this ... Some of these speakers may very well be dead against having a series with so few female speakers.

The list of Sponsors for their most recent meeting includes Google, Facebook, Microsoft and Yahoo. Time to pressure those companies and the other sponsors to drop sponsorship for this organization and their meeting.

UPDATE #2 4:00 PM. I have been told that there are active efforts underway by some members of the community to fix the underrepresentation of women as invited speakers in this meeting series. Stay tuned.

And in response to some comments from some of the CSHL Meeting people I decided to look into the past meetings in the same history of science series and was saddened with the incredibly low # of female speakers at all the meetings in this series. So I posted about that ...

And had more discussions on Twitter where CSHL made some claims about these History of Science meetings being a special case (not buying their argument, just reporting what they said).

And I thought I could have a relaxing Fourth of July weekend not spending my time dealing with Cold Spring Harbor Meetings. And then, well, I got an email from CSHL that I just looked at a few minutes ago. This email invited me to one of their "CSHL Asia Conferences".

I clicked on the link and when to the meeting site: Biological Rhythms and sadly I got sucked into YAMMM (yet another mostly male meeting) land. Here are the details on the organizers and presenters as far as I could sort out. I have labelled people I infer to be likely male in yellow and likely female in green. (I note I accept that a binary male vs. female representation of gender is less than ideal but I think in general this is a useful thing to look and to make some hypotheses for to assess meetings).

Organizers:

Carla Green, UT Southwestern, USA

Michael Hastings, MRC Laboratory of Molecular Biology, UK

Joseph Takahashi, HHMI/UT Southwestern, USA

Hiroki Ueda, University of Tokyo/RIKEN, Japan

Han Wang, Soochow University, China

Speakers

Joseph Takahashi, HHMI/UT Southwestern Medical Center, USA

Ravi Allada, Northwestern University, USA

Joseph Bass, Northwestern University Feinberg School of Medicine, USA

Deborah Bell-Pedersen, Texas A&M University, USA

Nicolas Cermakian, Douglas Mental Health University Institute, CANADA

Xinnian Dong, Duke University, USA

Yoshitaka Fukada, University of Tokyo, JAPAN

Carla Green, The University of Texas Southwestern Medical Center, USA

Jinhu Guo, Sun Yat-Sen University, China

Fang Han, Peking University People’s Hospital of Beijing, CHINA

Qun He, China Agricultural University, China

John Hogenesch, University of Pennsylvania School of Medicine, USA

Zhili Huang, Fudan University, China

Takao Kondo, Nagoya University/Div. of Biological Science, JAPAN

Katja Lamia, The Scripps Research Institute, USA

Cheng Chi Lee, University of Texas Health Science Center Houston, USA

Yi Liu, UT Southwestern Medical Center, USA

Chang Liu, Nanjing Normal University, China

Hugh Piggins, University of Manchester, UNITED KINGDOM

Till Roenneberg, Ludwig-Maximilians-University Munich, GERMANY

Louis Ptacek, HHMI/University of California San Francisco, USA

Hiroki Ueda, RIKEN Kobe Institute, JAPAN

David Virshup, Duke-NUS Graduate Medical School, SINGAPORE

Han Wang, Soochow University, China

Charles Weitz, Harvard Medical School, USA

David Whitmore, University College London, UNITED KINGDOM

Ying Xu, Soochow University, China

Xiaodong Xu, Hubei Normal University, China

Erquan Zhang, National Institute of Biological Sciences, China

Zhangwu Zhao, China Agricultural University, China

So that is 30 speakers. Only 29 of which could I find information on the web to make a hypothesis of gender. Of those 29, I inferred 6 - or 20% to be female. That is just really low for biological sciences. I am sorry Cold Spring Harbor but you are just not doing a good enough job with diversity. Scratch that, you are doing a bad job. Sad to see.